During conventional pharmacologic dose corticosteroid therapy, ACTH production is inhibited with subsequent suppression of cortisol production by the adrenal cortex. Recovery time for normal HPA activity is variable depending upon the dose and duration of treatment. During this time the patient is vulnerable to any stressful situation. Although it has been shown that there is considerably less adrenal suppression following a single morning dose of prednisolone (10 mg) as opposed to a quarter of that dose administered every six hours, there is evidence that some suppressive effect on adrenal activity may be carried over into the following day when pharmacologic doses are used. Further, it has been shown that a single dose of certain corticosteroids will produce adrenal cortical suppression for two or more days. Other corticoids, including methylprednisolone, hydrocortisone, prednisone, and prednisolone, are considered to be short acting (producing adrenal cortical suppression for 1¼ to 1½ days following a single dose) and thus are recommended for alternate day therapy.
The most common side effect of topical corticosteroid use is skin atrophy. All topical steroids can induce atrophy, but higher potency steroids, occlusion, thinner skin, and older patient age increase the risk. The face, the backs of the hands, and intertriginous areas are particularly susceptible. Resolution often occurs after discontinuing use of these agents, but it may take months. Concurrent use of topical tretinoin (Retin-A) % may reduce the incidence of atrophy from chronic steroid applications. 30 Other side effects from topical steroids include permanent dermal atrophy, telangiectasia, and striae.
Q: Please, explain the use of calcium channel blockers in glaucoma treatment. Do they replace other medications such as beta-blockers or are they used in conjunction with other glaucoma medication? Is it more dangerous to the patient to use calcium channel blockers when the patient is being treated for other health problems such as heart disease?
A: Calcium channel blockers represent an entirely new approach to the treatment of glaucoma. Hopefully, the advent of these drugs marks only the beginning of a trend in finding new approaches to the treatment of glaucoma over the coming years.
Previously, the only form of treatment of glaucoma has involved lowering intraocular pressure (IOP), even when IOP is normal to begin with. Although the evidence is not all in yet, calcium channel blockers have been reported to increase blood flow to the eye and to stabilize the visual field. Thus, instead of lowering IOP (although they appear to do this also), calcium channel blockers increase the resistance of the eye to glaucomatous damage. Because they represent an entirely new approach to the treatment of glaucoma, they do not replace other medications that are used in conjunction with them.
There are different types of calcium channel blockers. Some primarily affect the strength with which the heart contracts, while others affect peripheral blood vessels, making them dilate so that more blood can pass through. The calcium channel blockers used in the treatment of glaucoma ideally would be those which increase blood flow to the brain, since the eye and the brain share a common blood supply.
It remains to be determined just which patients will be helped and which will not be helped, or even perhaps harmed, by calcium channel blockers. Calcium channel blockers can also lower blood pressure, and a low blood pressure predisposes to glaucomatous damage. Therefore, we do not use these drugs at the present time in patients who have low blood pressure, but only in those with normal or high blood pressure. The patient's internist or family physician should be consulted with regard to the treatment plan.